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Volume 344:925926

March 22, 2001

Number 12

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Ris Fa!tors for "ree!la#$sia

An estimated 50,000 women per year worldwide die from preeclampsia. Preeclampsia is more likely to develop in women whose mothers had preeclampsia than in women whose mothers did not.1 The daughters-in-law of women who had preeclampsia are also somewhat more likely to have preeclampsia than other women. According to data on appro imately 1.! million "irths in #orway,$ a woman who "ecomes pregnant "y a man who has already had a child with a different woman who had preeclampsia during that pregnancy has a risk of preeclampsia that is nearly twice as high as that of a woman whose partner does not have such a history. %n this issue of the Journal, &splin and colleagues' report that men who were themselves "orn of pregnancies complicated "y preeclampsia are twice as likely to have a child who is the product of a pregnancy complicated "y preeclampsia as are men who were "orn after a normal pregnancy. There thus seems to "e "oth a maternally transmitted and a paternally transmitted genetic predisposition to preeclampsia. The a"ility to study this predisposition is hampered "y the o"vious fact that preeclampsia is a disease of pregnancy and no markers for the disorder have yet "een identified in nonpregnant women, let alone men. An increased risk of preeclampsia may "e associated with gene polymorphisms, "ut none have "een identified. A tendency to hypercoagula"ility predisposes women to preeclampsia.( )everal polymorphisms in genes that control the clotting cascade have "een identified, although the data linking particular polymorphisms to preeclampsia are contradictory, presuma"ly "ecause of differences in populations. )ome studies have reported that a polymorphism in the angiotensinogen gene is more fre*uent in women with preeclampsia than in normotensive pregnant women.5 +ther candidate genes currently under investigation include those involved in lipid meta"olism and "iotransformation "y en,ymes5- those that control the ./A system seem not to have a role in causing preeclampsia.5 The identification of underlying risk factors for preeclampsia is made more difficult "y the pro"a"ility that the diagnosis covers more than one condition, which follow a "roadly common pathway from the second trimester to delivery. The clinical

presentation of preeclampsia is highly varia"le, and there are differences "etween the clinical definition and those used in research.0 %n some women, pregnancy unmasks latent hypertensive disease. 1omen who have relatively high systolic or diastolic "lood pressure "efore $0 weeks of pregnancy are at increased risk for preeclampsia. The cutoff levels are lower than those normally considered to indicate hypertension. 2or e ample, in a study of nearly 1',000 women in the first half of pregnancy, those with a systolic "lood pressure of 1'0 mm .g or higher were nearly four times as likely to have preeclampsia as women with a systolic "lood pressure lower than 110 mm .g.! The association with diastolic "lood pressure is weaker. 1omen with pree isting chronic hypertension also have an increased risk of preeclampsia. Parado ically, white women who have hypertension alone during pregnancy 3gestational hypertension4 are more likely to have chronic hypertension in later life than those who have "oth hypertension and su"stantial proteinuria 3$5 or more "y dipstick test4 during pregnancy 6 the com"ination that defines classic preeclampsia.7 8onversely, women who have preeclampsia are more likely to have ischemic heart disease in later life than those who have gestational hypertension alone.9 1omen who remain normotensive during all pregnancies are less likely than women in the general population to have hypertension in later life. #ulliparity has "een confirmed as a risk factor for preeclampsia, in "oth large-scale epidemiologic studies! and detailed clinical studies.! A change of partner for a second or su"se*uent pregnancy causes a woman:s risk to return to nearly the values associated with nulliparity, suggesting a poorly defined immunologic contri"ution to the condition. Appro imately (0 to 50 percent of multiparous women with a diagnosis of preeclampsia have had preeclampsia during a previous pregnancy. %f the condition re*uired delivery at or "efore '$ weeks: gestation in a previous pregnancy, the odds ratio for recurrence increases to more than (0.! 1omen with a "ody-mass inde 3the weight in kilograms divided "y the s*uare of the height in meters4 greater than $5 early in pregnancy are more likely to "ecome hypertensive than those with a lower "ody-mass inde , "ut whether the increased risk is for gestational hypertension or preeclampsia is uncertain. 8onversely, women with a very low "ody-mass inde have a decreased risk of gestational hypertension.10 Among nulliparous women, "lack women have a risk of preeclampsia that is twice as high as that of white women11- they are also more likely to have hypertension that is independent of pregnancy. A curious "ut consistent finding is that women who smoke cigarettes have a lower risk of preeclampsia than women who do not smoke, even when confounders are carefully e cluded.1$ The "a"ies of cigarette smokers are smaller than those of nonsmokers, presuma"ly "ecause of to"acco-related interference with the transfer of placental nutrients, and their average "lood pressures are lower. Pree isting dia"etes mellitus is another risk factor for preeclampsia- incidence rates range from 9 percent up to 00 percent among women with pree isting dia"etic nephropathy.1' ;ultiple pregnancy dou"les the risk of preeclampsia. The placental mass is large in "oth dia"etes and multiple pregnancy, and the placenta is at the heart of the pro"lem. )evere preeclampsia can occur without a fetus 3i.e., in a molar pregnancy4. <elivery is the ultimate cure. .ypo ia or reperfusion in=ury during placentation might account for the endothelial damage that is increasingly recogni,ed as playing a part in the pathogenesis of preeclampsia.5 Platelet activation in the first

trimester is an indicator of risk. Pree isting conditions associated with endothelial damage, such as hyperhomocysteinemia,5 dia"etes, and insulin resistance, would thus "e e pected to "e associated with, and indeed are associated with, an increased risk of preeclampsia. &nvironmental factors may also contri"ute to the development of preeclampsia. 2or e ample, the high incidence of preeclampsia in many poor countries suggests that an inade*uate diet may "e a risk factor. The dietary inade*uacies that have "een proposed as relevant include deficiencies of calcium, ,inc, vitamins 8 and &, and n>' essential fatty acids. ?ecommendations for a sensi"ly "alanced diet during pregnancy should "e part of routine antenatal care. The roots of preeclampsia lie in very early pregnancy, "ut as yet we have no relia"le means of identifying women who are at risk "efore the condition is esta"lished. &ducating all pregnant women a"out how to recogni,e danger signals would help, since clinically dangerous preeclampsia can develop very rapidly. @ood o"stetrical practice will identify known risk factors "ut will not ena"le physicians to determine the Arisk valueA for a particular pregnancy. That is a matter for the future. 2iona Broughton Pipkin, <.Phil, 2.?.8.+.@. University of Nottingham Nottingham NG7 2UH, United Kingdom

Referen!es
1. 8hesley /8. .ypertension in pregnancyC definitions, familial factor, and remote prognosis. Didney %nt 1970-17C$'(-$(0. E1e" of )cienceFE;edlineF $. /ie ?T, ?asmussen ), Brun"org ., @=essing .D, /ie-#ielson &, %rgens /;. 2etal and maternal contri"utions to risk of pre-eclampsiaC population "ased study. B;G 1997-'10C1'('-1'(!. E2ree 2ull Te tF '. &splin ;), 2ausett ;B, 2raser A, et al. Paternal and maternal components of the predisposition to preeclampsia. # &ngl G ;ed $001-'((C70!7!$. E2ree 2ull Te tF (. /ockwood 8G. .erita"le coagulopathies in pregnancy. +"stet @ynecol )urv 1999-5(C!5(-!05. E8ross?efFE;edlineF 5. Broughton Pipkin 2, ?o"erts G;. .ypertension in pregnancy. G .um .ypertens $000-1(C!05-!$(. E8ross?efFE;edlineF 0. .iggins G?, de )wiet ;. Blood-pressure measurement and classification in pregnancy. /ancet $001-'5!C1'1-1'5. E8ross?efFE1e" of )cienceFE;edlineF !. Hdegard ?A, Iatten /G, #ilsen )T, )alvesen DA, Austgulen ?. ?isk factors and clinical manifestations of pre-eclampsia. BG+@ $000-10!C1(10-0.

7. Brown ;A, Buddle ;/. %nade*uacy of dipstick proteinuria in hypertensive pregnancy. Aust # J G +"stet @ynaecol 1995-'5C'00-'09. E1e" of )cienceF E;edlineF 9. Gonsdottir /), Arnsgrimsson ?, @eirsson ?T, )igvaldson ., )igfusson #. <eath rates from ischemic heart disease in women with a history of hypertension in pregnancy. Acta +"stet @ynecol )cand 1995-!(C!!$!!0. E1e" of )cienceFE;edlineF 10. )aftlas A, 1ang 1, ?isch ., 1oolson ?, .su 8, Bracken ;. Prepregnancy "ody mass inde and gestational weight gain as risk factors for preeclampsia and transient hypertension. Ann &pidemiol $000-10C(!5-(!5. 11. )i"ai B;, &well ;, /evine ?G, et al. ?isk factors associated with preeclampsia in healthy nulliparous women. Am G +"stet @ynecol 199!-1!!C100'-1010. E8ross?efFE1e" of )cienceFE;edlineF 1$. Kiong K, 1ang 2/, <avidge )T, et al. ;aternal smoking and preeclampsia. G ?eprod ;ed $000-(5C!$!-!'$. E1e" of )cienceFE;edlineF 1'. )i"ai B;. ?isk factors, pregnancy complications, and prevention of hypertensive disorders in women with pregravid dia"etes mellitus. G ;atern 2etal ;ed $000-9C0$-05. E8ross?efFE;edlineF

This article has been cited b other articles:

&scher, @., 8ristiano, ;., 8ausevic, ;., Baumann, ;., 2rey, 2. G., )ur"ek, <., ;ohaupt, ;. @. 3$0094. .igh aldosterone-to-renin variants of 8LP11B$ and pregnancy outcome. Nephrol Dial Transplant $(C 17!0-17!5 EA"stractF E2ull Te tF ;istry, .. <., 1ilson, I., ?amsay, ;. ;., )ymonds, ;. &., Pipkin, 2. B. 3$0074. ?educed )elenium 8oncentrations and @lutathione Pero idase Activity in Preeclamptic Pregnancies. Hypertension 5$C 771-777 EA"stractF E2ull Te tF )k=aerven, ?., Iatten, /. G, 1ilco , A. G, ?onning, T., %rgens, /. ;, /ie, ?. T. 3$0054. ?ecurrence of pre-eclampsia across generationsC e ploring fetal and maternal genetic components in a population "ased cohort. B J ''1C 7!!EA"stractF E2ull Te tF Games, P ?., #elson-Piercy, 8. 3$00(4. ;anagement of hypertension "efore, during, and after pregnancy. Heart 90C 1(99-150( E2ull Te tF Pouta, A., .artikainen, A.-/., )ovio, M., @issler, ;., /aitinen, G., ;c8arthy, ;. %., ?uokonen, A., &lliott, P., Garvelin, ;.-?. 3$00(4. ;anifestations of ;eta"olic )yndrome After .ypertensive Pregnancy. Hypertension ('C 7$57'1 EA"stractF E2ull Te tF ;ello, @., Parretti, &., @ensini, 2., )ticchi, &., ;ecacci, 2., )carselli, @., @enuardi, ;., A""ate, ?., 2atini, 8. 3$00'4. ;aternal-2etal 2low, #egative &vents, and PreeclampsiaC ?ole of A8& %N< Polymorphism. Hypertension (1C 9'$-9'! EA"stractF E2ull Te tF

)k=aerven, ?., 1ilco , A. G., /ie, ?. T. 3$00$4. The %nterval "etween Pregnancies and the ?isk of Preeclampsia. N!J '(0C ''-'7 EA"stractF E2ull Te tF

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